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High blood pressure
Manuel L.
Fontes,Fun-Sun F.
Yao
(Translated by Ma Jiajia, Hao Yanhong, reviewed by Li Tianzuo, Wang Tianlong)
Beijing Tongren Hospital Affiliated to Capital Medical University/Xuanwu Hospital of Capital Medical University
Cases
Patient, male, 70 years old
Cholecystectomy
is intended for cholelithiasis.
Blood pressure 230/120mmHg, heart rate 60 beats / min, hematocrit 38%, blood sodium 140mEq/L, blood potassium 2.
7mEq/L
.
Medications include propranolol and hydrochlorothiazide
.
A.
Disease and differential diagnosis
1.
Definition and severity grading
of hypertension.
2.
Epidemiology of hypertension?
3.
What is the general classification of hypertension? List the causes
of various types of hypertension.
4.
What are the clinical types of hypertension?
5.
What is the pathophysiology of essential hypertension?
6.
What is the pathophysiological mechanism of isolated systolic hypertension with increased pulse pressure?
7.
What kind of damage can long-term hypertension cause to terminal organs?
8.
Are hypertensive patients at high risk of perioperative cardiac morbidity?
9.
Are perioperative brain and kidney complications related to subtypes of hypertension?
10.
Would you use controlled blood pressure lowering techniques for people with high blood pressure? How much should a patient's blood pressure be lowered from a safety perspective?
11.
What is the mechanism of action of antihypertensive drugs?
12.
Does the choice of antihypertensive drug affect the hemodynamic response during anesthesia induction, laryngoscopy, and endotracheal intubation?
13.
Does long-term application of ACE inhibitors have an effect on anesthesia induction?
Disease and differential diagnosis 01 Definition and severity grading of
hypertension.
Hypertension
is diagnosed when arterial pressure exceeds the normal high limit allowed for age, sex, and ethnicity.
According to the latest definition and description of blood pressure by the Joint Commission International on the assessment, detection and prevention of hypertension, the optimal blood pressure status for adults is less than 120 mmHg systolic blood pressure and less than 80 mmHg
diastolic blood pressure.
Table 10.
1 presents the classification of desirable, normal, and hypertension, as well as the classification of the
degree of hypertension.
The upper limit of normal blood pressure in children is as follows:
100/75mmHg Early adolescence
85/55mmHg infancy
70/45mmHg
It is worth mentioning that the new classification criteria for hypertension define and refine systolic hypertension and diastolic hypertension because they represent different pathophysiological mechanisms
.
Systolic hypertension is a hallmark of disease of the macrovascular system or atherosclerosis, and diastolic hypertension is secondary to diseases of the microvascular system, commonly referred to as blood vessels
with an inner diameter of less than 1 mm.
Hypertension can also be divided into hypertensive emergencies and hypertensive critical conditions
.
According to the JNC VII report, hypertensive crisis is defined as blood pressure above 180/120 mmHg and a risk of
end-organ damage or progressive end-organ damage.
A hypertensive emergency is defined as a severely elevated blood pressure without progressive end-organ damage
.
The epidemiology of hypertension depends on the ethnicity of the population and the criteria
for defining hypertension.
In a study of suburban whites in Framingham, nearly 1/5 had blood pressure above 160/95mmHg, and almost 1/2 had blood pressure above 140/90mmHg
.
It is more
common in non-white people.
With age, the probability of hypertension also increases, and about two-thirds of people with hypertension are older than 50 years old
.
Subtypes of hypertension are also affected
by age.
Young individuals have diastolic hypertension or a combination of diastolic and systolic hypertension, while older patients mostly have systolic hypertension
.
In 1983, the number of hypertensive patients in the United States was about 57.
7 million, more than
double the total number of hypertensive patients in 1960-1962.
Nearly 70 million Americans currently have high blood pressure
.
of various types of hypertension.
According to the subtype of hypertension: systolic hypertension, diastolic hypertension and wide pulse pressure hypertension (Table 10.
2).
In the past, only diastolic hypertension (essential hypertension) was recognized, but systolic hypertension is now increasingly emphasized and recognized, called isolated systolic hypertension (ISH).
ISH is the most common subtype
of hypertension in people over 60 years of age.
In fact, nearly 70% of hypertensive patients have ISH, and more than half have a large pulse pressure difference (>65mmHg) or an increase in pulse pressure (hyperpulse hypertension, PPH).
Isolated diastolic hypertension (IDH) is more common in patients younger than 50 years of age, and IDH is an important marker
of cardiovascular disease and mortality in this age group.
Some patients have both systolic and diastolic hypertension, known as a combination of systolic and diastolic hypertension
.
The range of systolic, diastolic, and pulse pressure that defines each subtype of hypertension is shown in Table 10.
1
.
Etiology of hypertension
● The cause of essential hypertension is unknown
.
● Renal hypertension: acute and chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney, diabetic nephropathy, hydronephrosis, renal vascular stenosis, renin-derived tumors, primary sodium retention
.
● Endocrine hypertension: adrenal-Cushing syndrome, essential hyperaldosteronism, hereditary adrenal hyperplasia, pheochromocytoma, acromegaly, hypothyroidism, carcinoid tumors, hyperthyroidism, oral contraceptives, cortisol hormones
.
● Neurogenic factors: psychological factors, increased intracranial pressure, spinal cord problems, familial autonomic abnormalities, lead poisoning, Guil-lain-Barre syndrome, sleep apnea
.
● Mixed: arterial coarctation, increased intravascular volume, gestational hypertension, polyarteritis nodosa, acute porphyria, hypercalcemia, alcohol and drug abuse, acute stress such as surgery
.
●"Vasoconstrict" hypertension: Common in medical patients with chronic renovascular hypertension, characterized by diastolic hypertension with normal systemic resistance or even decreased cardiac output and heart rate
.
●"Hyperdynamic" hypertension: occurs in patients after surgery and is characterized by acute systolic hypertension, increased pulse pressure, and increased
cardiac output, heart rate, and systemic vascular resistance.
The underlying mechanism of essential hypertension is unclear
.
It involves a large number of abnormal structures and states of the body, including heredity, malnutrition during the fetal period, abnormal sympathetic nervous system activity, malformations of cell membranes, excessive salt retention of the kidneys, variations in microcirculation, abnormal function of the inner cell membrane, hyperinsulinemia secondary to insulin resistance, excessive proliferation of blood vessels, regular changes in the renin-angiotensin system, and so on
.
There is increasing evidence that topical renin-angiotensin paracrine factors may influence the development and progression
of hypertension.
Nevertheless, its characteristic hemodynamic changes are as follows:
●Normal cardiac output and increased peripheral vascular resistance (SVR);
● Sympathetic hyperresponse caused by stress, such as endotracheal intubation;
● With the thickening of the blood vessel wall and the increase of the ratio of the thickness of the blood vessel wall to the inner diameter of the blood vessel, the blood pressure of vasoconstriction increases significantly, while the vasodilation blood pressure decreases
significantly.
With an increase in blood pressure levels, diseases of the cardiovascular system may appear
earlier with the acceleration of atherosclerosis.
If not treated systematically, nearly 50% of hypertensive patients will die of coronary heart disease or congestive heart failure (CHF), nearly 33% will have stroke, and 10%~15% will die of kidney failure
.
ISH is a manifestation
of atherosclerosis, which predominates the aorta, the aortic arteries and their major branches.
Both ISH and PPH reflect the hardening of blood vessels and represent the pulsating component of blood pressure, while mean arterial pressure (MAP) represents a static component
.
The systolic state of the ventricles, the amount of ejection, heart rate, and, most importantly, the compliance of the aortic arteries and the rate of the pulse wave all directly affect the contraction
of the heart.
With age and the influence of various related factors, such as diabetes, smoking, hypercholesterolemia and some genetic factors, the compliance of the aortic arteries decreases significantly (Figure 10.
1).
The end result is hardening of the arteries at all levels, which does not cushion the pressure load of the blood flow impingement, resulting in a significant increase
in systolic blood pressure.
Pulse wave (conduction) velocity has recently begun to attract attention because it is an important parameter
to characterize blood flow and stress physiology.
Under normal physiologic conditions, ejection is delivered to the periphery
in the form of transfer waves.
When it reaches the periphery, especially where there are branches, a reflected wave or a retrograde wave is generated, which travels to the aortic valve
.
The arrival of this wave usually overlaps with the onset of diastolic and thus increases the diastolic blood pressure component
.
However, with the aging of arteriosclerosis gradually intensifies, so that the peripheral transmission wave and reflection wave propagate faster, and the arterial reflection wave that comes back early in the late systolic stage increases the component of systolic blood pressure, so that the afterload increases
.
The loss of diastolic enhancement leads to a disproportionate increase in systolic and diastolic blood pressure, the former being higher and the latter relatively low, which is characteristic of
simple systolic hypertension with increased pulse pressure.
In principle, pulse pressure is also an indicator of the hardening of the blood vessel wall, and it is also a parameter
of the propagation and reflection ratio of pressure waves between arterial trees.
Almost half of patients with isolated systolic hypertension have a wide pulse pressure; Nevertheless, patients with combined hypertension with blood pressure within the normal range (systolic blood pressure < 140 mmHg) and low diastolic blood pressure and high systolic (> 140 mmHg) and diastolic blood pressure (> 90 mmHg) may have a wider pulse pressure (normal value is ≤ 40 mmHg).
Long-standing hypertension causes damage to terminal organs as follows:
Heart disease includes: left ventricular hypertrophy; angina or myocardial infarction; Arrhythmia; Congestive heart failure
.
Ocular diseases include: Hypertensive retinopathy and atherosclerotic retinopathy
due to changes in blood vessels in the fundus.
Kidney diseases include: kidney disease
.
Brain disorders include stroke or transient ischemic attack (TIA).
Vascular complications associated with hypertension may include three associated processes: pulsating blood flow, endothelial cell dysfunction, and smooth
muscle cell hypertrophy.
These three related processes may be responsible for arterioles and arteriosclerosis, which are common complications
of chronic hypertension.
Large blood vessels such as the aorta may be directly affected, as well as the risk of
aneurysms and arterial dissection.
As discussed earlier, complications associated with chronic hypertension should be classified
according to the subtype of hypertension.
The risk associated with cardiac, brain, and renal vascular disease
varies depending on the type of hypertension classified according to systolic, diastolic, and pulse pressure.
For example, diastolic hypertension is a good predictor of coronary heart disease in young patients; However, systolic and pulse pressure predict a higher
risk of stroke, coronary heart disease, and death in patients older than 60 years.
Patients with hypertension are at higher
risk of coronary heart disease, asymptomatic myocardial ischemia, congestive heart failure, and stroke.
However, whether preoperative hypertension means a higher incidence of the cardiovascular system during the perioperative period has been controversial
.
Some studies have shown that patients with hypertension who have not undergone systematic treatment before surgery, with poor or unstable blood pressure, are at greater risk of developing blood pressure instability, rhythm disturbances, myocardial ischemia, and transient neurological complications during surgery.
Some scholars have also proposed that preoperative hypertension predicts possible myocardial
infarction during surgery.
Still, Glodman and Caldera confirmed that mild to moderate hypertension did not increase the risk of
more serious events during surgery.
Conversely, preoperative hypertension may indicate moderate complications, such as blood pressure instability and myocardial ischemia
.
There is controversy
due to the large individual variability of people with hypertension.
The effect of hypertension on morbidity is mainly through a certain degree of damage to the terminal organs, rather than the manifestation of
hypertension itself.
Left ventricular hypertrophy, which means a state of long-term poor control of hypertension, with or without coronary heart disease, increases the risk of
myocardial ischemia due to an imbalance in the supply and demand of myocardial oxygen.
In the general population, ISH (systolic blood pressure greater than 140 mmHg, diastolic blood pressure less than 90 mmHg) has been recognized as a risk factor for cardiovascular complications, and treatment reduces the risk of
future stroke.
Recently, Aronson and Fontes found that among the various components of blood pressure, preoperative pulse pressure is an important factor
that independently and significantly affects stroke, kidney failure, and mortality after bypass transplantation in patients with coronary heart disease.
Neither ISH nor simple diastolic hypertension are predictors of vascular complications
.
This finding is consistent with longitudinal studies that elevated pulse pressure is more appropriate as a predictor of vascular complications than systolic or diastolic blood pressure
.
Interestingly, in both normal and hypertensive patients, an increase in pulse pressure of just 10 mmHg increases the risk of developing cardio-cerebral and renal diseases by 20% or more
.
Both systolic hypertension and wide pulse pressure are clearly associated
with intraoperative cerebrovascular accident and acute renal failure.
The brain, kidneys, and heart differ from other organs in that they receive a large amount of blood flow with low
resistance.
Correspondingly, pulsating loads (pulse pressure) are more likely to reach very high levels
.
If hypertension is not systematically treated and controlled for many years, endothelial damage and vascular remodeling will accelerate the progression of arteriosclerosis and arterial occlusion, which is the so-called risk factor for
cardiovascular and renal vascular complications.
Pulse pressure can also cause plaque to break off the aortic arteries and their major branches, leading to thromboembolism
.
In hypertensive patients, cerebral blood flow re-regulates to a higher range of changes than normal, protecting brain tissue from sudden increases in blood pressure but being susceptible
to hypotension.
Therefore, when blood pressure decreases sharply, hypertensive patients will have signs of cerebral ischemia at higher levels of hypertension than normal patients
.
High blood pressure accelerates cognitive decline with age
.
Hypertension, especially systolic hypertension, is an important risk factor
for initial or recurrent stroke and transient ischaemic attack due to extracranial vascular occlusion.
Chronic renal insufficiency is a common secondary change
in hypertension.
Patients with hypertension should have basal serum creatinine levels measured
.
Among the initial risk factors for heart disease, elevated serum creatinine levels [>3.
0 mg/dl (>265.
2 mmol/L)] are an independent risk factor
for perioperative cardiovascular morbidity and mortality.
This statement has been confirmed in the corrected heart disease risk index, and preoperative creatinine levels above 2.
0 mg/dl, or 176.
8 mmol/L, are one
of the six factors that increase the risk of the cardiovascular system.
Uncontrolled or untreated severe hypertension is a contraindication to controlled blood pressure reduction
.
However, controlled blood pressure lowering in patients with hypertension should be used
with caution.
Because cerebral blood flow self-regulation shifts to the right in patients with chronic hypertension, the bottom line level of controlled blood pressure lowering in hypertensive patients is higher than normal
.
However, after long-term treatment, the self-regulation curve of hypertensive patients tends to the left towards normal levels
.
Strangard found that the bottom line for self-regulation in patients with untreated or controlled severe hypertension was 113 mmHg, compared with 96 mmHg for those who had previously developed severe hypertension and were currently receiving treatment, compared with 73 mmHg
in the normal population.
The lowest mean blood pressure level in the tolerable asymptomatic hypoperfusion state is 65 mmHg in patients with severe hypertension, 53 mmHg in patients with hypertension under treatment, and 43 mmHg
in the normal population.
Although the self-regulation curve can tend to normal levels after treatment, many patients do not reach normal levels
even after 12 months of treatment.
Because we cannot measure the patient's level of self-regulation, a useful clinical guideline is that a 25% reduction in mean arterial pressure (MAP) reaches the bottom line of self-regulation, and a 55% reduction results in symptomatic cerebral hypostasis
.
Another recommendation is that systolic blood pressure should not be lower than the patient's normal diastolic blood pressure level
for controlled blood pressure.
It is worth mentioning that the blood pressure measured on the periphery does not represent the blood pressure of the central artery, which better reflects the actual blood pressure level
of the brain.
Recently, cerebral oximeters using near-infrared spectroscopy have been used to monitor blood oxygen saturation in the cerebral cortex
.
Cerebral oxygen saturation is a mixed venous oxygen saturation, of which 85% comes from the jugular vein and 15% from the arteries
.
It reflects the balance
between oxygen supply and demand in the brain.
Under stable anesthesia, there is no significant change
in the oxygen requirements of the brain.
Therefore, the oxygen saturation of the brain does not decrease unless the drop in blood pressure is below the lower limit
of its self-regulation.
Therefore, cerebral oximeters can be used to monitor the lower limit of self-regulation and ensure adequate cerebral oxygen saturation
.
However, for those patients with basal oxygen saturation close to 50%, the monitoring results of cerebral oxygen saturation vary greatly
.
In addition, monitoring results reflect only local oxygen saturation and may not be detected
at distal sites of ischemia.
It is worth mentioning that the thresholds for the upper and lower limits of systolic and diastolic blood pressure have not been determined
so far.
These boundaries are often chosen arbitrarily, and the association between intraoperative hypertension and outcomes as stated in the relevant papers is inconsistent
.
The lower limits covered in some papers come from a collection of
various types of hypertension.
In addition, existing vasoactive drugs do not selectively raise or lower systolic and diastolic blood pressure without affecting another part of
blood pressure.
Over the past few decades, a series of studies in humans have clearly demonstrated that morbidity and mortality are not directly related to the rise or fall of blood pressure, which has significantly affected
the unlimited trust in systolic and diastolic blood pressure.
In patients with diagnosed coronary heart disease (so-called old myocardial infarction), the mortality rate of coronary heart disease is directly related to diastolic blood pressure with U-shaped waves – often in
patients with very high or low diastolic blood pressure.
Unfortunately, the emphasis on intraoperative blood pressure management has focused attention on systolic blood pressure control to the neglect of diastolic blood pressure
.
This is especially true in patients with isolated systolic hypertension with increased pulse pressure, although their diastolic blood pressure is already relatively low
.
By lowering systolic blood pressure, diastolic blood pressure is further reduced, which leads to ischaemic complications
in some of the more sensitive vascular beds, such as the heart, brain, and kidneys.
Finally, peripheral arterial pressure does not necessarily reflect central pressure in addition to mean arterial pressure
.
In a small proportion of hypertensive patients, peripheral systolic and pulse pressure are much higher than central aortic pressure, so lowering peripheral blood pressure will result in a significant reduction
in perfusion pressure.
Antihypertensive drugs are divided into the following categories according to their different mechanisms of action:
Diuretics
These include thiazides (e.
g.
, hydrofluorothiazide), loop diuretics (e.
g.
, furosemide, ethacrylic acid), and potassium-sparing diuretics (e.
g.
, spironolactone, triamterene).
Diuretics lower blood pressure
by increasing the secretion of urine sodium and reducing plasma volume, extracellular fluid volume, and cardiac output.
Within 6~8 weeks, cardiac output returns to normal levels
.
The decrease in blood pressure is closely related to the decrease in peripheral resistance
.
Diuretics cause hypokalemia, hypomagnesemia, hyperuricemia, hyperlipidemia, hypercalcemia, and hyperglycemia
.
Intravenous furosemide may be appropriate
in patients with ST-segment changes, pulmonary edema, increased intracranial pressure, and hypertension.
Antiadrenergic drugs
● Central drugs: clonidine, dexmedetomidine and mivasidol
.
These drugs and metabolites are mainly α:receptor agonists
.
By stimulating the receptors of the vascular motor center A of the brain, the output
of the sympathetic nerve is reduced.
● Drugs acting on the periphery
● α receptor blockers
● A1 and alpha2 blockers – phenoxybenzamine (tabenezilin), phentolamine (pritidine)
● A receptor blockers - prazosin (prazosin hydrochloride), doxazosin mesylate (glycidyl ester) reduce peripheral resistance
by blocking A-mediated vasoconstriction, dilating arterioles and veins.
● β blockers – atenolol (tenoxamine), metoprolol (metoprolol tartrate), apolipoprotein (considol), indolol (propranol), propranolol (propranolol), esmolol (methyl phenylpropionate hydrochloride).
These drugs lower blood pressure
by slowing heart rate, myocardial contractility, reducing cardiac output, and lowering renin levels.
The decrease in blood pressure is not accompanied by reflex tachycardia and widening
of pulse pressure.
At the same time, it can also resist arrhythmias, inhibit ventricular and supraventricular pre-contractions
.
● A and β receptor blockers——— labetalol (saloxamine hydrochloride heart customizer).
● Endothelin receptor antagonist - acts on endothelin A and B receptors to block the action of endothelin-1, which is the most powerful factor of vasoconstriction and is mainly secreted
by vascular smooth muscle and endothelial cells.
Bosentan (A and B receptor antagonists) and thiophenecarboxamide (A receptor antagonists) are some of these drugs used to treat pulmonary hypertension and reduce heart failure
associated with hypertension.
Direct vasodilator drugs
Includes hydralazine, nitroprusside, nitroglycerin, and calcium channel blockers
.
These drugs directly reduce smooth muscle resistance and volumetric vascular tone to varying degrees
.
Dopaminergic agonists (DAs)
DAs are divided into two subtypes: DA∶ and DA∶: (1) excited DA; The receptor causes vasodilation and inhibits efficient sodium ion transport in the proximal tubule, leading to increased
urinary sodium excretion.
(2) Excitatory DA: receptors inhibit the release of norepinephrine and enhance the dilation
of peripheral blood vessels.
Fenodopam, a dopamine receptor (selective DA, receptor) agonist, is a systemic and renal vasodilator that offers significant advantages
as an injectable agent in the management of hypertensive crises and perioperative management.
Fenodopam for injection has a rapid onset of action without residual effect, and the half-life of removal in the body is about 10 minutes
.
The dosage concentration is 10 mg of the drug added to 250 ml of saline (40 gg/ml), and the recommended first dose is 0.
05 μg/(kg·min).
The effective dose of intravenous drip is 0.
025μg/(kg·min), which needs to be used every 10~15 minutes, and the maximum dose is 0.
5~0.
8μg/(kg·min).
Intravenous bolus administration is not recommended, and the incidence of reflex tachycardia is related
to the maximum speed of intravenous drip.
Unlike dopamine, the drug does not have a stimulant effect of a and β adrenergic, increasing the dose increases the dilating effect of blood vessels, but does not cause tachycardia or abnormal rhythmic tachycardia
.
Calcium channel blockers
The cardiovascular system effects of calcium channel blockers are described in
Table 10.
3.
These drugs lower blood pressure mainly by relaxing peripheral blood
vessels.
The secretion of renin and aldosterone is also reduced
.
Angiotensin-converting enzyme (ACE) inhibitors
Including captopril, enalapril, lisinopril, quinapril and ramipril
.
The renin-angiotensin system may begin with
Four pathways are inhibited, as shown in Figure 10.
2
.
These drugs inhibit the conversion
of inactivated Decapeptidin angiotensin I to the active octapeptide angiotensin II.
A decrease in angiotensin II levels can lower blood pressure
by inhibiting angiotensin II-mediated vasoconstriction and reducing aldosterone synthesis.
ACE inhibitors can also delay the degradation of an effective vasodilator (bradykinin), reduce the production of prostaglandins (mainly captopril), remodel the activity
of the adrenergic nervous system.
ACE inhibitors (angiotensin-converting enzyme inhibitors, ACEIs) have a significant effect of dilating arterial blood vessels, and their effect of reducing afterload has gradually become the basic drug
for the treatment of chronic heart failure.
Increasing cardiac output without reducing preload greatly improves survival
.
Angiotensin II receptor antagonist
Angiotensin II receptor antagonists or blockers (ARBs) target a third pathway antagonizing the renin-angiotensin-aldosterone system
.
Blocking the effect of angiotensin II leads to an increase
in plasma levels of renin, angiotensin I and angiotensin II.
However, the increase in this series of precursors did not outweigh the receptor blocking effect, as
evidenced by a decrease in blood pressure and the level of aldosterone in the blood plasma.
There may be some differences
between ACEIs and ARBs.
These include the following:
● ACE is a kininase that can be degraded into bradykinin
.
Therefore, inhibition of this enzyme with ACEI increases kinin levels, while ARBs do not
.
Elevated bradykinin levels also promote vasodilation and other benefits that ARBs do not
.
● ACEI inhibits AT by reducing the production of angiotensin II; and AT, the role of receptors; ARBs only suppress the
former.
Chronic agonist effects on AT:receptors may be beneficial
.
● In the heart, kidneys, and blood vessels, angiotensin II production is catalyzed by other enzymes (e.
g.
, gastric pancreatase) rather than ACE
.
ARBs can inhibit the effects of angiotensin II produced through this reaction process, while ACEI cannot
.
There is evidence that ARBs are more effective in the treatment of ISH and PPH, particularly when
combined with ACEIs and endothelin receptor inhibitors.
Other vasodilators
These include brain natriuretics, such as nesiritide mainly used to treat acute severe heart failure, to improve blood supply to the heart and reduce the signs and symptoms
of heart failure.
Recently, controversy
has emerged about the clinical efficacy of these drugs.
Importantly, there have been some reports of deterioration
in renal function in patients who have used nesirittide.
For patients with mild to moderate hypertension, there is little
difference in the pressure response to induction of anesthesia, laryngoscopy, and endotracheal intubation β choice of receptor blocker, calcium-channel blocker, ACEI, or diuretics.
Even untreated patients showed similar changes
.
On the other hand, anesthesia induction amplifies the hypotensive response in patients with poorly controlled blood pressure—depending on the degree of
reduction in intravascular volume based on vascular sympathetic tension.
As mentioned above, we should also focus on diastolic and pulse pressure, not just systolic blood pressure
.
Coriat et al.
reported that in hypertensive patients treated with ACEI drugs for a long time, it is crucial
to stabilize blood pressure during anesthesia induction when undergoing vascular surgery, taking the drug until the day of surgery.
If treatment with enalapril (long-acting ACE inhibitor) is continued preoperatively, very low plasma-converting enzyme levels will be monitored and an increased
hypotensive response will occur during induction.
If captopril (short-acting ACE inhibitor) is continued preoperatively, the degree of blood pressure drop at induction is lower than that with enalapril, but the degree of blood pressure reduction is enhanced compared with patients who discontinue captopril before surgery
.
For all patients whose ACEI is used until the day of surgery, hypotension can be easily corrected by applying a receptor agonist.
Temporary discontinuation of these two classes of ACEIs attenuates the hypotensive response to induction but does not cause abnormal blood pressure responses
during induction and intubation.
In short, the final view is to continue to use all antihypertensive drugs including the day of surgery, and resume their use
after surgery.
Many studies have shown that continued medication before surgery improves prognosis and vice versa
.
Finishing + typesetting / jingle balls hemp
